Big Sanyang
Introduction
Introduction The so-called "three-and-a-half-size" refers to two different results of "two-and-a-half-test of hepatitis B antigen" (referred to as two-and-a-half of hepatitis B). The first pair in "two halves" refers to surface antigens (HBsAg) and surface antibodies (anti-HBs), the second pair is E antigen (HBeAg) and E antibody (anti-HBe), and the third pair is the core. Antibody (anti-HBc) and core antigen (HBcAg). Since the core antigen has been fully assembled into hepatitis B virus in hepatocytes and there is no free core antigen in the serum, only half of the third pair, the core antibody, can be detected in the surrounding blood.
Cause
Cause
It is currently believed that the onset of hepatitis B is closely related to the immune status of the body.
After infection with hepatitis B virus, it will inevitably cause the body's immune response, resulting in different serum immunological markers. It is currently believed that the pathogenesis of hepatitis B is closely related to the body's immune response, especially the cellular immune response in the body, and the age characteristics of the body. Determine the maturity of the body's immune system, the infant's immune system is in a development process, at this time the ability to clear the virus is poor, so it is easy to be chronic and immune, the adult immune system is fully developed, it is easy to carry out immune clearance in a short period of time, Therefore, it is manifested as acute hepatitis B. When the body's immune function is low, incomplete immune tolerance, and HBV gene mutations evade immune clearance, it can also lead to chronic hepatitis. When the body is in a hypersensitivity reaction, a large number of antigen-antibody complexes are produced. The activation of the compensatory system, as well as the involvement of a large number of inflammatory factors, can lead to large pieces of hepatocyte necrosis, ie severe hepatitis.
Examine
an examination
Related inspection
Hepatitis B two-and-a-half liver function test
Laboratory examinations must be summarized and analyzed based on objective materials and medical examinations, and several possible diagnostics are proposed, and then further examinations are performed to confirm the diagnosis. Such as: 1 biochemical indicators, including ALT, AST, bilirubin, albumin and renal function; 2 blood routine, urine routine, blood sugar and thyroid function; 3 virological markers, including HBsAg, HBeAg, anti-HBe and HBV - baseline status or level of DNA; 4 for patients with middle-aged or older, should be electrocardiogram and blood pressure; 5 exclude autoimmune diseases; 6 urine human chorionic gonadotropin test to exclude pregnancy.
Diagnosis
Differential diagnosis
Drug-induced hepatitis
The characteristics are: 1 history of useful drugs, known to have a variety of drugs can cause different degrees of liver damage, such as isoniazid, rifampicin can cause similar clinical manifestations of viral hepatitis; long-term use of diacetate, methyl Dopa can cause slow-lived liver; chlorpromazine, methyltestosterone, arsenic, bismuth, ketoconazole, etc. can cause cholestatic hepatitis; 2 mild clinical symptoms, elevated ALT, eosinophils; 3 After the drug was stopped, the symptoms gradually improved and ALT returned to normal.
2. Cholelithiasis
There was a history of biliary colic, high fever chills, right upper quadrant pain, Murphy sign (Murphy sign), increased white blood cells, and increased neutrophils.
3. Primary biliary cirrhosis
The characteristics are: 1 middle-aged women are more common; 2 jaundice continues to be noticeable, itchy skin, often yellow tumor, hepatosplenomegaly is obvious, ALP is significantly elevated, most anti-mitochondrial antibodies are positive; 3 liver function damage is lighter; 4 hepatitis B The marker is negative.
4. Hepatolenticular degeneration (Wilson's disease)
There is often a family history, with extensive tremors of the limbs, increased muscle tone, a brown-green pigment ring at the edge of the cornea (KF ring), decreased copper and ceruloplasmin, increased urinary copper, and slow-lived hepatic copper and copper. Blue protein is significantly elevated.
5. Acute fatty liver during pregnancy
Most occur in the second trimester of pregnancy. The clinical features are: 1 acute onset of acute abdominal pain, amylase increased, like acute pancreatitis; 2 although there are heavy jaundice, serum direct bilirubin increased, but urinary bilirubin is often negative. Domestic reports of this phenomenon can also be found in acute severe hepatitis for reference; 3 often before the onset of liver failure, severe bleeding and renal dysfunction, ALT increased, but turbidity is normal; 4B ultrasound for fatty liver waveform To help early diagnosis, diagnosed by pathological examination. The pathological features are the enlargement of the hepatic lobule to the middle zone, the cytoplasm is filled with fat vacuoles, and there is no large hepatocyte necrosis.
6. Extrahepatic obstructive jaundice
Such as pancreatic cancer, common cholangiocarcinoma, chronic pancreatitis, etc. need to be identified.
